Separate DNA Pol II- and Pol IV-dependent pathways of stress-induced mutation during double-strand-break repair in Escherichia coli are controlled by RpoS

J Bacteriol. 2010 Sep;192(18):4694-700. doi: 10.1128/JB.00570-10. Epub 2010 Jul 16.

Abstract

Previous work showed that about 85% of stress-induced mutations associated with DNA double-strand break repair in carbon-starved Escherichia coli result from error-prone DNA polymerase IV (Pol IV) (DinB) and that the mutagenesis is controlled by the RpoS stress response, which upregulates dinB. We report that the remaining mutagenesis requires high-fidelity Pol II, and that this component also requires RpoS. The results identify a second DNA polymerase contributing to stress-induced mutagenesis and show that RpoS promotes mutagenesis by more than the simple upregulation of dinB.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism*
  • DNA Polymerase II / genetics
  • DNA Polymerase II / metabolism*
  • DNA Polymerase beta / genetics
  • DNA Polymerase beta / metabolism*
  • DNA Repair* / genetics
  • Escherichia coli / enzymology*
  • Escherichia coli / genetics*
  • Escherichia coli Proteins / genetics
  • Escherichia coli Proteins / metabolism*
  • Mutagenesis
  • Mutation / genetics
  • Sigma Factor / genetics
  • Sigma Factor / metabolism*
  • Signal Transduction / genetics
  • Signal Transduction / physiology*

Substances

  • Bacterial Proteins
  • Escherichia coli Proteins
  • Sigma Factor
  • sigma factor KatF protein, Bacteria
  • DNA Polymerase II
  • DNA Polymerase beta